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1 rth dose of PCV (if they experienced chronic graft vs host disease).
2 ing technology, decreasing the likelihood of graft vs host disease.
3 arrow, and there was no evidence of clinical graft vs host disease.
4 rm tolerance or developed late-onset chronic graft-vs-host disease.
5 adiation toxicity, but also protects against graft-vs-host disease.
6 sponses, such as platelet refractoriness and graft-vs-host disease.
7 e chimerism without causing acute or chronic graft-vs-host disease.
8 emely limited repertoire of Ags can initiate graft-vs-host disease.
9 from kidneys of animals with murine chronic graft-vs-host disease.
10 similar to lesions associated with cutaneous graft-vs-host disease.
11 e donor engraftment without acute or chronic graft-vs-host disease.
12 with continued stable donor chimerism and no graft-vs-host disease.
13 in the treatment of allograft rejection and graft-vs-host disease.
14 unity of both donor and host T cells without graft-vs-host disease.
15 t disease, demonstrating that LC can trigger graft-vs-host disease.
16 of pathological changes in a human model of graft-vs-host disease.
17 tions and tumors as well as autoimmunity and graft-vs-host disease.
18 of T cell-mediated autoimmune disorders and graft-vs-host disease.
19 on tolerance across MHC disparities, without graft-vs-host disease.
20 mune disease that at times resembles chronic graft-vs-host disease.
21 ic BMT by contributing to the development of graft vs. host disease.
22 in autoimmune diseases, transplantation, and graft vs. host disease.
23 nsplantation, but can cause life-threatening graft-vs.-host disease.
25 drome (22 eyes), Sjogren syndrome (11 eyes), graft-vs-host disease (2 eyes), dry eye after keratomile
28 the PBL of a patient suffering from chronic graft-vs-host disease after bone marrow transplant from
29 gen-primed effector memory T cells to induce graft-vs-host disease after bone marrow transplantation
30 tural suppressor" T cells protect hosts from graft-vs-host disease after the infusion of allogeneic b
31 ne studies have found acute gastrointestinal graft-vs-host disease (aG-GVHD) to be associated with in
32 een associated with increased rates of acute graft-vs-host disease (aGVHD) after allogeneic hematopoi
33 l of CTL development, parent-into-F(1) acute graft-vs-host disease (AGVHD), to evaluate this issue.
35 ne alone, were markedly impaired in inducing graft-vs-host disease alloresponses to MHC class II disp
36 nd thereby cause chronic graft rejection and graft-vs-host disease among MHC identical individuals.
37 could serve as an ideal strategy to prevent graft-vs-host disease and allograft rejection or to trea
38 tocompatibility (H) Ag disparities result in graft-vs-host disease and chronic solid allograft reject
39 uman allogeneic bone marrow transplantation, graft-vs-host disease and graft rejection can occur even
40 BB represents a new approach to altering the graft-vs-host disease and graft-vs-leukemia effects of a
41 erapeutic for organ transplant recipients or graft-vs-host disease and is an approved therapeutic for
42 ll (DC) functions and regulates experimental graft-vs-host disease and other immune-mediated diseases
43 l populations have the potential to suppress graft-vs-host disease and stimulate antitumor responses.
44 treated T cells lost their ability to induce graft-vs-host disease and, instead, prevented other pare
46 erred into semiallogeneic mice fail to cause graft-vs-host disease, and when injected into syngeneic,
47 te chimerism; incidence of acute and chronic graft-vs-host disease; and sickle cell-thalassemia disea
48 ls in cyclosporin A (CSA)-induced autologous graft-vs-host disease are recent thymic emigrants (RTEs)
49 , neutrophil recovery, and acute and chronic graft-vs-host disease, as ascertained by transplant cent
50 8%; HR, 0.77; 95% CI, 0.48-1.23), or chronic graft-vs-host disease at 1-year (cumulative incidence, 2
52 ing symptoms or not having symptoms of acute graft-vs-host disease between 25 and 161 days after HCT.
53 cells (RBCs) prevents transfusion-associated graft-vs-host disease but also exacerbates storage lesio
54 lone is characterized by a decreased risk of graft-vs-host disease but increased incidence of engraft
55 rventions to control autoimmune diseases and graft vs. host disease, but oversuppression of these pat
58 parent-into-F(1) (p-->F(1)) model of chronic graft-vs-host disease (cGVHD) in which lupus-like humora
61 d BMT-related therapeutic exposures, chronic graft-vs-host disease (cGVHD), and posttransplant immuno
65 nocytes had 40% early mortality due to acute graft-vs-host disease compared with no deaths among reci
66 ve pretreatment regimens, graft failure, and graft-vs-host disease complicate the utility of BMT for
67 er prospective cohort study from the Chronic Graft-vs-Host Disease Consortium including 9 medical cen
68 replaced by donor cells, exhibit marked skin graft-vs-host disease, demonstrating that LC can trigger
69 vs 85%; HR, 0.94; 95% CI, 0.73-1.22), acute graft-vs-host disease grades III-IV at 100 days (cumulat
70 been detected in mice, the ability to induce graft vs host disease (GVHD) after bone marrow transplan
71 c stroke, acute myocardial infarction (AMI), graft vs host disease (GvHD), and acute respiratory dist
72 risk for grades II to IV and III to IV acute graft vs host disease (GVHD), chronic GVHD, transplant-r
76 t-vs-leukemia (GVL) response but also induce graft-vs-host disease (GVHD) after allogeneic bone marro
78 approach being evaluated for the control of graft-vs-host disease (GVHD) after allogeneic bone marro
79 cids like butyrate and protection from acute graft-vs-host disease (GvHD) after allogeneic stem cell
80 at could be important for the development of graft-vs-host disease (GVHD) after bone marrow transplan
81 ner as naive T cells with respect to causing graft-vs-host disease (GVHD) and facilitating engraftmen
83 NF/TNFR2 interactions ameliorates intestinal graft-vs-host disease (GVHD) and Th1 cytokine responses
85 F(1)) model of acute or chronic (lupus-like) graft-vs-host disease (GVHD) as a model of either a CTL-
87 been used to elucidate the immunobiology of graft-vs-host disease (GVHD) following allogeneic bone m
90 -vs-leukemia (GVL) activity, but also induce graft-vs-host disease (GVHD) in recipients conditioned w
92 he parent-into-immunocompetent-F(1) model of graft-vs-host disease (GVHD) induces immune dysregulatio
99 ry tests for the diagnosis and monitoring of graft-vs-host disease (GVHD) is hampered by a lack of kn
108 h between several mechanisms responsible for graft-vs-host disease (GVHD) protection in anti-CD3epsil
109 ive treatment for leukemia and lymphoma, but graft-vs-host disease (GVHD) remains a major complicatio
112 nce was also demonstrated to be operative in graft-vs-host disease (GVHD) responses against BALB.B-de
114 MT can mediate a potent GVL effect with less graft-vs-host disease (GVHD) than would be observed if g
116 anti-TNF-alpha mAb to mice undergoing acute graft-vs-host disease (GVHD) using the parent-into-F(1)
118 he parent-into-F1 model of acute and chronic graft-vs-host disease (GVHD) was used as an example of i
119 ents, allogeneic HCT recipients with chronic graft-vs-host disease (GvHD) were at increased risk of f
120 ics, risk factors for, and impact of chronic graft-vs-host disease (GVHD) were evaluated in a consecu
121 hed donor bone marrow (BM) graft exacerbated graft-vs-host disease (GVHD) when DLI was administered a
122 dels, this ex vivo sFasL treatment abrogated graft-vs-host disease (GVHD) while sparing donor T cells
123 implicated in the pathophysiology of chronic graft-vs-host disease (GVHD), and phase 2 trials suggest
124 immunotoxins (ITs) in the therapy of cancer, graft-vs-host disease (GvHD), autoimmune diseases, and A
125 tissue damage during allograft rejection and graft-vs-host disease (GVHD), but its role in supporting
126 quired for initiating T cell-dependent acute graft-vs-host disease (GVHD), but the role of APCs in th
127 has a major role in the development of acute graft-vs-host disease (GVHD), Fas ligand-deficient (gld)
129 parent-into-F(1) (P-->F(1)) model of chronic graft-vs-host disease (GVHD), using wild-type or TRAIL-d
130 , and ICOS regulate the development of acute graft-vs-host disease (GVHD), we wished to assess if BTL
131 Tg mice developed autoreactive skin disease (graft-vs-host disease (GVHD)-like skin lesions) while K1
151 ession on host APCs is essential to initiate graft-vs-host disease (GVHD); however, critical APC subs
152 tment (median, 68.3%) associated with severe graft-vs-host disease (GvHD; 62 vs 0% with TCDBM alone).
157 tacking healthy host tissues, termed chronic graft-vs-host disease, has become a more common phenomen
158 , 35.08 [95% CI, 3.90-315.27]), grade III/IV graft-vs-host disease (HR, 16.50 [95% CI, 2.67-102.28]),
159 responsible for chronic graft rejection and graft vs host disease in solid tissue and bone marrow tr
160 SOT was organ failure related to intractable graft-vs-host disease in 16 children (36.3%), acute or c
161 activity of donor T cells without increased graft-vs-host disease in both MHC- and minor histocompat
163 ent approval of an MSC therapy for pediatric graft-vs.-host disease in the United States, marking the
164 sion by human Tregs in a model of xenogeneic graft-vs.-host disease induced by the transfer of human
165 Similarly, in an in vivo mouse model of graft-vs-host disease, infusion of CAR-Tregs conferred a
166 a recipient alloantigen, thereby preventing graft-vs-host disease initiated by a TCR-transgenic T ce
167 ate that tolerance to CSA-induced autologous graft-vs-host disease is actively mediated by CD25+CD4+
168 the nephritogenic T cell response in chronic graft-vs-host disease is autoreactive in nature and may
169 the fate of alloreactive T cell effectors in graft-vs-host disease, Ld-specific CD8+ T cells from C57
170 uncommon, consisting of oral lichen planus, graft-vs-host disease-like colitis, and pure red cell ap
174 he same two loci identified with the chronic graft-vs-host disease model, excluding the Cr2 region.
177 ds ratio, 11.3; P < .01), acute (grade >/=2) graft-vs-host disease (odds ratio, 8.2; P < .02) and mis
179 in 'classic' ARDS, and discusses studies in graft-vs.-host disease, one of the few licensed indicati
182 ations include vascular barrier dysfunction, graft-vs-host disease, platelet activation, ischemia, an
184 Factors such as primary disease, chronic graft-vs-host disease, prolonged immunosuppression, radi
185 which may account, in part, for the partial graft-vs-host disease protective effect of anti-CD40L mA
187 iverse as erythema nodosum leprosum, chronic graft-vs-host disease, rheumatoid arthritis, and sarcoid
188 oughly characterize a murine sclerodermatous graft-vs-host disease (Scl GVHD) model for scleroderma t
194 .9]; P = .01; higher better) and Lee chronic graft-vs-host disease symptom scores (13.1 [1.5] vs 19.3
195 urrent paradigm, we find that, in a model of graft-vs-host disease, the immunotherapeutic effect of c
196 display antiviral activity without inducing graft-vs-host disease; therefore, we determined whether
197 imates were calculated for acute and chronic graft-vs-host disease, toxicities, achievement of full d
198 ine bone marrow (BM) NK T cells can suppress graft-vs-host disease, transplant rejection, and MLRs.
199 aluated pretransplant conditioning regimens, graft-vs-host disease treatment, or radiotherapy as expe
200 atment with immunosuppressive medication for graft-vs-host disease, treatment with rituximab in the p
202 tioning regimen, and presence of significant graft vs. host disease was not found to influence outcom
204 and mechanical ventilation; grade 3/4 acute graft-vs-host disease was associated with all-cause mort
206 a CD8(+) T cell adoptive transfer model for graft-vs-host disease, we demonstrate that a potent type
207 ents, allogeneic BMT recipients with chronic graft-vs-host disease were at increased risk for esophag
209 demonstrated in a parent-into-F(1) model of graft-vs-host disease, where dual TCR T cells comprised